Interleukin 4 Reduces Brain Hyperexcitability after Traumatic Injury by Downregulating TNF-α, Upregulating IL-10/TGF-β, and Potential Directing Macrophage/Microglia to the M2 Anti-inflammatory Phenotype
— Macrophage/microglia are activated after Traumatic brain injury (TBI), transform to inflammatory phenotype (M1) and trigger neuroinflammation, which provokes epileptogenesis. Interleukin-4 (IL-4) is a well-known drive of macrophage/microglia to the anti-inflammatory phenotype (M2). We tested effec...
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| Veröffentlicht in: | Inflammation 2023-10, Vol.46 (5), p.1810-1831 |
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| creator | Radpour, Mozhdeh Khoshkroodian, Bahar Asgari, Tara Pourbadie, Hamid Gholami Sayyah, Mohammad |
| description | —
Macrophage/microglia are activated after Traumatic brain injury (TBI), transform to inflammatory phenotype (M1) and trigger neuroinflammation, which provokes epileptogenesis. Interleukin-4 (IL-4) is a well-known drive of macrophage/microglia to the anti-inflammatory phenotype (M2). We tested effect of IL-4 on speed of epileptogenesis, brain expression of inflammatory and anti-inflammatory cytokines, and lesion size in TBI-injured male rats. Rats underwent TBI by
Controlled Cortical Impact
. Then 100 ng IL-4 was injected into cerebral ventricles. One day after TBI, pentylenetetrazole (PTZ) kindling started and development of generalized seizures was recorded. The lesion size, cell survival rate, TNF-α, TGF-β, IL-10, and Arginase1 (Arg1) was measured in the brain 6 h, 12 h, 24 h, 48 h, and 5 days after TBI. Astrocytes and macrophage/microglia activation/polarization was assessed by GFAP/Arg1 and Iba1/Arg1 immunostaining. TBI-injured rats were kindled by 50% less PTZ injections than control and sham-operated rats. IL-4 did not change kindling rate in sham-operated rats but inhibited acceleration of kindling rate in the TBI-injured rats. IL-4 decreased damage volume and number of destroyed neurons. IL-4 stopped TNF-α whereas upregulated TGF-β, IL-10, and Arg1 expressions. Iba1/Arg1 positive macrophage/microglia was notably increased 48 h after IL-4 administration. IL-4 suppresses TBI-induced acceleration of epileptogenesis in rats by directing TBI neuroinflammation toward an anti-inflammatory tone and inhibition of cell death. |
| doi_str_mv | 10.1007/s10753-023-01843-0 |
| format | Article |
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Macrophage/microglia are activated after Traumatic brain injury (TBI), transform to inflammatory phenotype (M1) and trigger neuroinflammation, which provokes epileptogenesis. Interleukin-4 (IL-4) is a well-known drive of macrophage/microglia to the anti-inflammatory phenotype (M2). We tested effect of IL-4 on speed of epileptogenesis, brain expression of inflammatory and anti-inflammatory cytokines, and lesion size in TBI-injured male rats. Rats underwent TBI by
Controlled Cortical Impact
. Then 100 ng IL-4 was injected into cerebral ventricles. One day after TBI, pentylenetetrazole (PTZ) kindling started and development of generalized seizures was recorded. The lesion size, cell survival rate, TNF-α, TGF-β, IL-10, and Arginase1 (Arg1) was measured in the brain 6 h, 12 h, 24 h, 48 h, and 5 days after TBI. Astrocytes and macrophage/microglia activation/polarization was assessed by GFAP/Arg1 and Iba1/Arg1 immunostaining. TBI-injured rats were kindled by 50% less PTZ injections than control and sham-operated rats. IL-4 did not change kindling rate in sham-operated rats but inhibited acceleration of kindling rate in the TBI-injured rats. IL-4 decreased damage volume and number of destroyed neurons. IL-4 stopped TNF-α whereas upregulated TGF-β, IL-10, and Arg1 expressions. Iba1/Arg1 positive macrophage/microglia was notably increased 48 h after IL-4 administration. IL-4 suppresses TBI-induced acceleration of epileptogenesis in rats by directing TBI neuroinflammation toward an anti-inflammatory tone and inhibition of cell death.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-023-01843-0</identifier><identifier>PMID: 37259014</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Anti-Inflammatory Agents ; Astrocytes ; Biomedical and Life Sciences ; Biomedicine ; Brain - metabolism ; Brain Injuries, Traumatic - pathology ; Cell activation ; Cell death ; Cell size ; Cell survival ; Cytokines ; Epilepsy ; Genotype & phenotype ; Glial fibrillary acidic protein ; Immunology ; Inflammation ; Interleukin 10 ; Interleukin 4 ; Interleukin-10 - metabolism ; Interleukin-4 - metabolism ; Internal Medicine ; Kindling ; Macrophages ; Macrophages - metabolism ; Male ; Microglia ; Microglia - metabolism ; Neuroinflammatory Diseases ; Pathology ; Pentylenetetrazole ; Pharmacology/Toxicology ; Phenotype ; Phenotypes ; Rats ; Rheumatology ; Seizures ; Transforming Growth Factor beta - metabolism ; Transforming growth factor-b ; Traumatic brain injury ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-α ; Ventricles (cerebral)</subject><ispartof>Inflammation, 2023-10, Vol.46 (5), p.1810-1831</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-d9c912614a5e86e731e0626952acfaddb0f93e8e2c09b8261a8ae3f1e86aed553</citedby><cites>FETCH-LOGICAL-c375t-d9c912614a5e86e731e0626952acfaddb0f93e8e2c09b8261a8ae3f1e86aed553</cites><orcidid>0000-0001-6315-6254 ; 0000-0003-2463-8087 ; 0000-0003-0603-2444 ; 0000-0003-1668-6820 ; 0000-0002-7634-7428</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10753-023-01843-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10753-023-01843-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37259014$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Radpour, Mozhdeh</creatorcontrib><creatorcontrib>Khoshkroodian, Bahar</creatorcontrib><creatorcontrib>Asgari, Tara</creatorcontrib><creatorcontrib>Pourbadie, Hamid Gholami</creatorcontrib><creatorcontrib>Sayyah, Mohammad</creatorcontrib><title>Interleukin 4 Reduces Brain Hyperexcitability after Traumatic Injury by Downregulating TNF-α, Upregulating IL-10/TGF-β, and Potential Directing Macrophage/Microglia to the M2 Anti-inflammatory Phenotype</title><title>Inflammation</title><addtitle>Inflammation</addtitle><addtitle>Inflammation</addtitle><description>—
Macrophage/microglia are activated after Traumatic brain injury (TBI), transform to inflammatory phenotype (M1) and trigger neuroinflammation, which provokes epileptogenesis. Interleukin-4 (IL-4) is a well-known drive of macrophage/microglia to the anti-inflammatory phenotype (M2). We tested effect of IL-4 on speed of epileptogenesis, brain expression of inflammatory and anti-inflammatory cytokines, and lesion size in TBI-injured male rats. Rats underwent TBI by
Controlled Cortical Impact
. Then 100 ng IL-4 was injected into cerebral ventricles. One day after TBI, pentylenetetrazole (PTZ) kindling started and development of generalized seizures was recorded. The lesion size, cell survival rate, TNF-α, TGF-β, IL-10, and Arginase1 (Arg1) was measured in the brain 6 h, 12 h, 24 h, 48 h, and 5 days after TBI. Astrocytes and macrophage/microglia activation/polarization was assessed by GFAP/Arg1 and Iba1/Arg1 immunostaining. TBI-injured rats were kindled by 50% less PTZ injections than control and sham-operated rats. IL-4 did not change kindling rate in sham-operated rats but inhibited acceleration of kindling rate in the TBI-injured rats. IL-4 decreased damage volume and number of destroyed neurons. IL-4 stopped TNF-α whereas upregulated TGF-β, IL-10, and Arg1 expressions. Iba1/Arg1 positive macrophage/microglia was notably increased 48 h after IL-4 administration. IL-4 suppresses TBI-induced acceleration of epileptogenesis in rats by directing TBI neuroinflammation toward an anti-inflammatory tone and inhibition of cell death.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents</subject><subject>Astrocytes</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain - metabolism</subject><subject>Brain Injuries, Traumatic - pathology</subject><subject>Cell activation</subject><subject>Cell death</subject><subject>Cell size</subject><subject>Cell survival</subject><subject>Cytokines</subject><subject>Epilepsy</subject><subject>Genotype & phenotype</subject><subject>Glial fibrillary acidic protein</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Interleukin 10</subject><subject>Interleukin 4</subject><subject>Interleukin-10 - metabolism</subject><subject>Interleukin-4 - metabolism</subject><subject>Internal Medicine</subject><subject>Kindling</subject><subject>Macrophages</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Microglia</subject><subject>Microglia - metabolism</subject><subject>Neuroinflammatory Diseases</subject><subject>Pathology</subject><subject>Pentylenetetrazole</subject><subject>Pharmacology/Toxicology</subject><subject>Phenotype</subject><subject>Phenotypes</subject><subject>Rats</subject><subject>Rheumatology</subject><subject>Seizures</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>Transforming growth factor-b</subject><subject>Traumatic brain injury</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-α</subject><subject>Ventricles (cerebral)</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kc1u1DAQxyMEokvhBTggS1w4NKw_1k58LC1tV9qFCm3PkZNMsl4SJ7UdwT4WPAfimRi65UMcOPhr5jf_GeufJM8Zfc0ozeaB0UyKlHJcLF_g_iCZMZmJlMtMPUxmVCiaCq2zo-RJCDtKaa5z8Tg5EhmXmrLFLPm2dBF8B9NH68iCfIB6qiCQN97g-2o_gofPlY2mtJ2Ne2IapMnGm6k30VZk6XaT35NyT86HT85DO3UYdy3ZvLtIv385ITfjX8HlKmV0vrnE1NcTYlxNrocILlrTkXProbqj1qbyw7g1LczXFq9tZw2JA4lbIGtOTpFPrWs60-MMA3a_3oIbIs76NHnUmC7As_vzOLm5eLs5u0pX7y-XZ6ertBKZjGmtK824YgsjIVeQCQZUcaUlN1Vj6rqkjRaQA6-oLnMETW5ANAxhA7WU4jh5ddAd_XA7QYhFb0MFXWccDFMoeM6ZEppyjejLf9DdMHmH0yGVSSVyqhRS_EDhd0Pw0BSjt73x-4LR4qfXxcHrAr0u7rwuKBa9uJeeyh7q3yW_zEVAHICAKdeC_9P7P7I_AAXtuEU</recordid><startdate>20231001</startdate><enddate>20231001</enddate><creator>Radpour, Mozhdeh</creator><creator>Khoshkroodian, Bahar</creator><creator>Asgari, Tara</creator><creator>Pourbadie, Hamid Gholami</creator><creator>Sayyah, Mohammad</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-6315-6254</orcidid><orcidid>https://orcid.org/0000-0003-2463-8087</orcidid><orcidid>https://orcid.org/0000-0003-0603-2444</orcidid><orcidid>https://orcid.org/0000-0003-1668-6820</orcidid><orcidid>https://orcid.org/0000-0002-7634-7428</orcidid></search><sort><creationdate>20231001</creationdate><title>Interleukin 4 Reduces Brain Hyperexcitability after Traumatic Injury by Downregulating TNF-α, Upregulating IL-10/TGF-β, and Potential Directing Macrophage/Microglia to the M2 Anti-inflammatory Phenotype</title><author>Radpour, Mozhdeh ; 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Macrophage/microglia are activated after Traumatic brain injury (TBI), transform to inflammatory phenotype (M1) and trigger neuroinflammation, which provokes epileptogenesis. Interleukin-4 (IL-4) is a well-known drive of macrophage/microglia to the anti-inflammatory phenotype (M2). We tested effect of IL-4 on speed of epileptogenesis, brain expression of inflammatory and anti-inflammatory cytokines, and lesion size in TBI-injured male rats. Rats underwent TBI by
Controlled Cortical Impact
. Then 100 ng IL-4 was injected into cerebral ventricles. One day after TBI, pentylenetetrazole (PTZ) kindling started and development of generalized seizures was recorded. The lesion size, cell survival rate, TNF-α, TGF-β, IL-10, and Arginase1 (Arg1) was measured in the brain 6 h, 12 h, 24 h, 48 h, and 5 days after TBI. Astrocytes and macrophage/microglia activation/polarization was assessed by GFAP/Arg1 and Iba1/Arg1 immunostaining. TBI-injured rats were kindled by 50% less PTZ injections than control and sham-operated rats. IL-4 did not change kindling rate in sham-operated rats but inhibited acceleration of kindling rate in the TBI-injured rats. IL-4 decreased damage volume and number of destroyed neurons. IL-4 stopped TNF-α whereas upregulated TGF-β, IL-10, and Arg1 expressions. Iba1/Arg1 positive macrophage/microglia was notably increased 48 h after IL-4 administration. IL-4 suppresses TBI-induced acceleration of epileptogenesis in rats by directing TBI neuroinflammation toward an anti-inflammatory tone and inhibition of cell death.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>37259014</pmid><doi>10.1007/s10753-023-01843-0</doi><tpages>22</tpages><orcidid>https://orcid.org/0000-0001-6315-6254</orcidid><orcidid>https://orcid.org/0000-0003-2463-8087</orcidid><orcidid>https://orcid.org/0000-0003-0603-2444</orcidid><orcidid>https://orcid.org/0000-0003-1668-6820</orcidid><orcidid>https://orcid.org/0000-0002-7634-7428</orcidid></addata></record> |
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| ispartof | Inflammation, 2023-10, Vol.46 (5), p.1810-1831 |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Animals Anti-Inflammatory Agents Astrocytes Biomedical and Life Sciences Biomedicine Brain - metabolism Brain Injuries, Traumatic - pathology Cell activation Cell death Cell size Cell survival Cytokines Epilepsy Genotype & phenotype Glial fibrillary acidic protein Immunology Inflammation Interleukin 10 Interleukin 4 Interleukin-10 - metabolism Interleukin-4 - metabolism Internal Medicine Kindling Macrophages Macrophages - metabolism Male Microglia Microglia - metabolism Neuroinflammatory Diseases Pathology Pentylenetetrazole Pharmacology/Toxicology Phenotype Phenotypes Rats Rheumatology Seizures Transforming Growth Factor beta - metabolism Transforming growth factor-b Traumatic brain injury Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-α Ventricles (cerebral) |
| title | Interleukin 4 Reduces Brain Hyperexcitability after Traumatic Injury by Downregulating TNF-α, Upregulating IL-10/TGF-β, and Potential Directing Macrophage/Microglia to the M2 Anti-inflammatory Phenotype |
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